Possible Effect of Abscisic Acid on Nitric Oxide in Isoproterenol-Induced Myocardial Infarction in Rats. | ||||
| Bulletin of Egyptian Society for Physiological Sciences | ||||
| Article 2, Volume 40, Issue 2, June 2020, Page 17-30 PDF (647.08 K) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/besps.2019.17609.1035 | ||||
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| Authors | ||||
Mona Gaber Elhadidy  1; Mahmoud Mohammed Elalfy2; lashin saad3
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| 1Department of Medical Physiology, Faculty of Medicine, Mansoura University, Egypt. | ||||
| 2Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Mansoura University, Egypt. | ||||
| 3Department of Medical Physiology, Faculty of Medicine, Mansoura University & Hours University, Egypt. | ||||
| Abstract | ||||
| The aim of this study was to find out the possible role nitric oxide (NO) due to its nature as a second messenger in stress responses in the cardioprotective effect of the abscisic acid (ABA) in isoproterenol (ISO) -induced myocardial infarction in rats. Material and method: Thirty male rats distributed into: normal control group, myocardial infarction (MI) group, and MI group treated with ABA for one week. The cardiac effect of ABA on ISO-induced MI was evaluated by ECG, measuring mean arterial pressure, markers of heart injury in serum, levels of lipid peroxidation, and antioxidants in heart tissue, observing pathological changes of tissue, and indirect detection of NO was performed. Results: Compared with the MI group, it was found that ABA could ameliorated ISO-induced disturbances in the ECG pattern and in mean arterial pressure. Moreover, the concentration of creatine kinase MB (CK-MB), lactate dehydrogenase (LDH), troponinI (CTn-I), nitrite and nitrate in the serum all decreased in the MI+ABA group. The activities of catalase (CAT), and the content of reduced glutathione (GSH) in heart increased, on the contrary, the content of malondialdehyde (MDA) and iNOS was decreased. In addition, the histopathologic examination showed that pathological changes in the myocardium that was observed in the MI group, was reduced in the group treated with ABA. Conclusion: ABA protected myocardium against damage caused by an ISO through inhibition of lipid peroxidation, prevent the cytotoxic actions of the excessive NO release, and restored near normal architecture and function of myocardial. | ||||
| Keywords | ||||
| Abscisic acid; Isoproterenol; Myocardial Infarction; Nitric oxide | ||||
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